In contrast, the study by Nishikawa et al demonstrating generation of “Treg-resistant” CD8+ cells used activated, tetramer-purified, antigen-specific CD8+ T cells in their suppression assays.[19] Based on these data, it is possible that a population of activated, tumor-specific CD8+ T cells from DTA-1-treated B16-bearing TDLN might be similarly “Treg-resistant.” While we did not demonstrate that GITR ligation directly modulated suppression or resistance to suppression, we did observe a reproducible increase in the intra-tumor effector function of tumor specific pmel-1 T cells. This evidence concerns the gene CD8A and neoplasm.